Study On Membrane Electrical Properties Of The Somatic Nociceptive Neurons Of Anterior Cingulate Gyrus

Pain is one of the most common symptom of patients with disease. But, there is not an ideal treatmentmethod of pain. Therefore, the research of pain mechanisms is important for pain relieve. Somatic pain andvisceral pain are different in types and qualities. Compared with visceral pain, somatic pain is accuratelylocalized, mild pain results in small emotional reactions and its perception of pain intensity. But, the precisemechanism of the perception differences between somatic and visceral pain remains unclear.Anterior cingulate gyrus (ACG) is components of limbic system and an important center of algesia.ACG is involved in both reception and modulation of somatic and visceral pain. Our previous study showsthat both visceral nociceptive neurons (VNNs) and visceral non-nociceptive neurons (VNNNs) havedifferent electrophysiological and membrane electrical properties. Therefore, we presumed that somaticnociceptive neurons (SNNs) and VNNs are different neurons. Therefore, it is necessary to study thecomplex mechanisms of reaction mode, function characteristics of a single SNNs and VNNs project to thecerebral cortex, and it will provide a new experimental evidence of perception between somatic and visceralpain. there is no reports about the difference between SNNs and VNNs. In order to investigate themembrane electrical properties of SNNs in ACG, we adopted the intracellular potential recording techniquesof glass microelectrode in vivo and the method of injecting a series of different intensity polarizing currentinto the neurons in ACG, and then compared the membrane electrical properties between SNNs and VNNsin ACG.In this study, we randomly selected57male or female cats, weighting from2.0kg to3.5kg.188neurons which produced evoked responses to electrical stimulation of SN were called SN stimulus-relativeneurons. According to the latency of the SN evoked responses, the SN stimulus-relative neurons weredivided into SNNs (91.49%) with a long latency (≥50ms) SN evoked responses and somatic non-nociceptive neurons (SNNNs,8.51%) with a short latency (<50ms) SN evoked responses. The evokedresponse of the SNNs have the specificities with high threshold (0.4～0.5mA), long latency (≥50ms),more complex reactive patterns, long time after effect, and inhibited by intravenous injection of morphine.Whereas the evoked response of the SNNNs have the specificities with low threshold(0.1～0.2mA), shortlatency (<50ms), and not inhibited by intravenous injection of morphine. The results that the evokedresponses of the contralateral ACG neurons were caused by electric stimulation of SN further proved thatSN afferent information could reach the contralateral ACG, and the contralateral ACG was one of the cortical areas of SN afferent projection.The results showed that less than0.2nA of hyperpolarizing current intensity injected into SNNs orSNNNs in ACG resulted in smaller the membrane potential of ACG SNNs or SNNNs, and then slowlyrestored to the resting level. With the gradual increase in hyperpolarizing current intensity, the amplitude ofmembrane potential hyperpolarization increased gradually in ACG SNNs or SNNNs. After injected thecurrent, it showed a backward jump slow depolarization wave, and sometimes some spikes in the slowdepolarization wave were triggered, namely anode blocking excitatory response. When depolarizing currentintensity injected into SNNs or SNNNs in ACG was less than0.2nA, only the local membrane potential ofACG SNNs or SNNNs became slowly depolarizing. With the gradual increase in depolarizing currentintensity (≥0.6nA) injected into SNNs or SNNNs in ACG, SNNs or SNNNs in ACG were discharged, andthe frequency of discharge of SNNs or SNNNs in ACG was gradually increasing, and the high frequencyaction potentials appeared on the slow depolarization wave of SNNs or SNNNs in ACG. But whendepolarizing current intensity injected into SNNs or SNNNs in ACG was more than4nA, the frequency ofdischarge of SNNs or SNNNs in ACG was no longer increasing, or displaying a downward trend. Whendepolarizing current intensity injected into SNNs or SNNNs in ACG was more than1nA, the amplitude ofdischarge of SNNs or SNNNs in ACG was gradually decreasing. Models of discharge of SNNs and SNNNsin ACG were different. Compared with SNNNs, adaptability of SNNs to current was poor，and thefrequency and amplitude of discharges of SNNs were significantly stronger (p<0.01). When depolarizingcurrent intensity injected into SNNs in ACG was gradually increasing, the change of frequency andamplitude of discharge of SNNs was more apparent. These results suggested that there is difference betweenmembrane electrical reaction of SNNs and SNNNs in ACG, and the adaptability of SNNs to current is lowerthan that of SNNNs, which might be the membrane electrical basis for characteristics of somatic painperception such as not easy to adapt.The present experiment observed the I-V curves of ACG SNNs and SNNNs were “S” shapes. When theabsolute value of polarizing current intensity injected into SNNs or SNNNs in ACG was less than1.0nA,theI and V of I-V curve of ACG SNNs or SNNNs was a linear correlation（rVNNs=0.99, rNVNNs=0.99） withoutsignificant difference. When the absolute value of polarizing current intensity injected into both was morethan1.0nA, ACG SNNs or SNNNs showed a certain inward or outward rectification effect. But therectification effect of SNNs was stronger than that of SNNNs (P<0.05), and the membrane resistance (Rm)of SNNs decreased quickly. These results suggested there are differences between the I-V curves and thestructures of cell membrane of ACG SNNs and SNNNs. The present experimental data showed that the Rm, membrane capacity (Cm) and time constant (τ) ofSNNs were higher than those of SNNNs (p<0.05or p<0.01). The results further proved there was differencebetween the membrane electrical properties of SNNs and SNNNs in ACG, which suggested there are somedifferences in the cell membrane structure and cell size. Whereas the present experimental data showed thatthe Rm, Cm and τ of SNNs were lower than Rm (19.62±2.01m，n=10), Cm (29.52±1.04PF) and τ(5.76±0.80ms) of VNNs (p<0.05or p<0.01) reported previously by our laboratory, which indicated thatcompared with somatic nociceptive information transmission, visceral nociceptive information transmissionspeed is slower, transmission duration is longer, and visceral nociceptive neurons is insensitive,not easilyexcited. This may be the membrane electrical basis for difference in characteristics between somatic andvisceral pain perception.